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Oral Leukoplakia REVIEW ARTICLE Roy G et al.: Oral Leukoplakia REVIEW ARTICLE Oral Leukoplakia: An Insight Gigi Roy1, Anu Vijayan2, Shamji Shajahan3, Anuja S4, Rashmi Elizabeth Mathen5 Correspondence to: 1, 3,4,5-Post Graduate, Department of Oral Medicine and Radiology, Mar Baselios Dr. Gigi Roy, Department of Oral Medicine and Dental College, Kothamangalam, Ernakulam(Dist), Kerala, India. 2-Senior Radiology, Mar Baselios Dental College, Lecturer,Department of Oral Medicine and Radiology, Mar Baselios Dental Kothamangalam, Kerala, India College, Kothamangalam, Ernakulam(Dist), Kerala, India. Contact Us: www.ijohmr.com ABSTRACT Leukoplakia is the most common oral white lesion that is classified under potentially malignant disorder affecting oral mucosa. It is significant as it has a high risk of malignant transformation. This article reviews the epidemiology, etiology and pathogenesis, clinical features and clinical variants, diagnosis, differential diagnosis, malignant potential, histopathological features, and treatment. KEYWORDS: Potentially Malignant Disorder, Smoking, Malignant, Dysplasia, Leukoplakia, Oral Cancer asasINTRODUCTIONss than elsewhere 6 . Prevalence in India is 0.2-4.9 percent.6,7 Earlier clinical presentations of the oral cavity that are Oral leukoplakia is usually seen in middle aged people, recognized as precancerous were classified into two broad and its prevalence is higher with age. About 90% of oral groups like lesions and conditions1, with the following leukoplakias are associated with the use of tobacco/areca definitions: a precancerous lesion is a morphologically nut and remaining 10% are idiopathic. Males are more altered tissue in which oral cancer is more likely to occur often affected than females probably owing to the greater than in its apparently normal counterpart, and a prevalence of tobacco use by males. The buccal mucosa precancerous condition is a generalized state associated is affected in 25% of cases, the mandibular gingiva in with a significantly increased risk of cancer. But now all 20%, the tongue in 10%, the floor of the mouth in 10%, 6 clinical presentations that carry a risk of cancer come and other oral sites account for the remainder. under the term ‗potentially malignant disorders‘ to reflect their widespread anatomical distribution.2 ETIOLOGY AND PATHOGENESIS Leukoplakia (leukos meaning white; plakia meaning Tobacco: The etiology of OL is considered patch) is the most common potentially malignant disorder multifactorial, but smoking is appreciated to be a affecting the oral mucosa. The term leukoplakia was frequently involved factor. It is much more common 8 coined by Schwimmer in 1877. It has been defined as ―a among smokers than among nonsmokers . Either in predominantly white lesion of the oral mucosa that smoke or smokeless (chew) form is the main etiologic cannot be characterized as any other definable lesion, not factor. Smoke/ Smokeless form release carcinogens that associated with any physical or chemical causative agent either bind to epithelial DNAs and cause damage to DNA except the use of tobacco‖.3 causing mutation and resulting in dysplasia or malignant transformation of a cell or highly reactive radicals are Warnakulasuriya et al.in 2007 defined Leukoplakia formed which damage cell membrane, DNA should be used to recognize white plaques of fragmentation, tissue damage and alter cellular questionable risk having excluded (other) known diseases 2 antioxidant defense system and causes keratinocyte or disorders that carry no increased risk for cancer . stimulation resulting in hyperkeratinization. Heat from According to Warnakulasuriya et al. , the new concept of smoke and frictional irritation from chew form cause OL shall acknowledge white lesions with a questionable keratinocyte stimulation as a protective response causing risk of being an OL, being excluded any other hyperkeratinization9. pathologies or known disorders which do not present potential malignant risks such as candidiasis, lupus Alcohol- Individuals with leukoplakia generally consume erythematosus, lichen planus, hairy leukoplakia, frictional alcohol and tobacco together. Consuming alcohol alone keratosis, nicotinic stomatitis, and leukoedema.4 was not associated with development of leukoplakia. But it was found to have some synergistic effect with tobacco 3 EPIDEMIOLOGY in the development of both leukoplakia and oral cancer . Mechanical trauma- Continuous trauma in the form of Global prevalence of oral leukoplakia range from 0.5% to chronic cheek biting, ill-fitting dentures, etc. have also 3.46%, and of the rates of carcinomatous transformation 3 found to be causative factors for leukoplakia. of oral leukoplakia from 0.7% to 2.9%.5 Oral leukoplakia is more prevalent in India where persons smoke and Sanguinaria- Herbal extract sanguinaria which is used in practice the habit of tobacco and areca nut chewing more mouthwashes and toothpastes was found to develop How to cite this article: Roy G, Vijayan A, Shajahan S, Anuja S, Mathen RE. Oral Leukoplakia: An Insight. Int J Oral Health Med Res 2018;5(1):57-61. International Journal of Oral Health and Medical Research | ISSN 2395-7387 | MAY-JUNE 2018 | VOL 5 | ISSUE 1 57 Roy G et al.: Oral Leukoplakia REVIEW ARTICLE leukoplakia (Sanguinaria-associated keratosis). Even after Phase 4- Erythroleukoplakia/ Speckled/ Non homogenous stopping usage of this product, the lesion did not subside. leukoplakia The commonest site was maxillary vestibule and alveolar Pindborg11 mucosa.3 Homogeneous leukoplakia Candida causing leukoplakia- Candida releases Non homogeneous leukoplakia nitrosamine specific proto-oncogene and also efficiently 12 converts ethanol into carcinogenic acetaldehyde in Bailoor and Nagesh alcohol drinker. This has a synergistic effect with tobacco Speckled leukoplakia and non speckled leukoplakia which increases dysplasia or leukoplakia. Studies show Homogenous, Ulcerative, Speckled that even after elimination of surface mycosis after Reversible / irreversible administration of antifungals, the leukoplakia persisted. WHO (1980)11 Malignant transformation of candida infected Homogeneous leukoplakias was high, suggesting candida association as 9 Smooth a significant risk factor for oncogenesis. Furrowed(Fissured) Papilloma virus- The role of Human Papilloma Virus Ulcerated (HPV) in the etiology as well as oncogenesis of oral Non Homogeneous leukoplakia have been under extensive molecular biology Nodulospeckled and virology studies. HPV type 16 was isolated in oral Preleukoplakia usually begins as thin, grey or greyish leukoplakias and carcinomas. In Proliferative Verrucous 9,10 3 white plaque that may appear somewhat translucent. leukoplakia (PVL), HPV 16 and 18 were demonstrated. Homogenous leukoplakia is thick smooth whitish with Epstein barr virus (EBV)- The role of EBV in oral cracked mud appearance and leathery consistency. These leukoplakias was not found in any of the studies even are asymptomatic with a very low risk of malignancy.9,10 though it was found to be associated with etiology of oral squamous cell carcinomas. If there is any role of EBV in Granular/ Nodular/ Verruciform/ Rough leukoplakia oral leukoplakias studies carrying out on a larger sample are more severe form with surface irregularities like may help us. 3 nodular or granular or pointed papillary projections.9,10 Non- homogenous leukoplakia consists of erythematous CLINICAL FEATURES area seen on the whitish plaque. It is suggestive of further progression of lesion towards malignancy. Patients Leukoplakia is seen in middle age and older age with a 9,10 peak incidence in fifth to seventh decades. It is more complain of pain, itching and discomfort. prevalent in males than females. Generally, it is seen as Proliferative verrucous leukoplakia is a subtype of gray, white or yellowish white in color. OL present on the verrucous leukoplakia characterized by an aggressive floor of the mouth, soft palate, and tongue are considered evolution, a multifocal appearance, resistance to as high-risk lesions, while, they may be considered as treatment, higher degree of recurrence and a high rate of 4 low malignant risk when occurs in other areas . Common malignant transformation8. Hansen et al. (1985) first sites are buccal mucosa and commissures, followed by described PVL as a distinct clinical form of OL. WHO lips, tongue, palate, alveolar ridge, floor of mouth, soft described the high rate of malignant transformation of 7 palate and gingiva. PVL. It is multifocal progressive lesions, commonly seen in women. The most affected area was the lower gingival, tongue, buccal mucosa, and alveolar ridge.3,13 CLINICAL VARIANTS Axell et al.,19849 There are four stages that have been described in the development of PVL, initially as a simple hyperkeratosis 1. Etiological without epithelial dysplasia, followed by verrucous Tobacco-associated leukoplakia hyperplasia, verrucous carcinoma, and finally Idiopathic leukoplakia conventional carcinoma.14,15,16 Ghazali et al.,17suggested 2. Clinically the following criteria for the diagnosis of PVL: Homogenous 1. The lesion should start as homogeneous leukoplakia Non homogenous with histopathological findings of dysplasia Erosive 2. Later in it should show verrucous areas Nodular 3. From single lesion, it should progress to multiple Verrucous lesions at the same or different site 4. It should progress later into different histological Bouquot Je & Whitaker10 stages. Phase 1- Thin or Preleukoplakia 5. It should show recurrence after treatment Phase 2- Homogenous/ Fissured/
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